More than one gene within the major histocompatibility complex of the mouse, H-2, has been shown to influence the susceptibility of mice to viral leukemogenesis, and evidence exists for at least three different mechanisms involved in this effect. The first is the induction of tumor-specific cytolytic T cells in response to recognition of an H-2/viral protein molecular complex formed on tumor cell surfaces. The second is the regulation of the capacity of the host to recognize and respond to viral antigens by H-2-linked immune response genes. A possible third is the influence of H-2 type on the cessation of virus production (replication suppression) by virus-induced tumor cells. Studies of each of these possible mechanisms will be carried out using cultured cell lines derived from Friend virus or Gross virus-induced tumors, or both, of mice of the H-2-congenic BALB/c lines.